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CBL cases Flashcards

1
Q

General enquiry for paediatric patients

A
  1. feeding
  2. activity
  3. sleep
  4. temperament
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2
Q

Important features in a paediatric history specifically

A

Maternal history:
- antenatal: scan abnormalities, infections
- perinatal: gestation, delivery, complications
- postnatal: time in SCBU, neonatal sepsis
Developmental history
Immunisations
SHx: smokers in the house, social worker involvement, family and school life
FHx: congenital heart/hip/kidney disease, consanguinity

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3
Q

Which murmurs in children are never innocent

A

Diastolic

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4
Q

Common urine dip finding in febrile children

A

Raised protein - transient proteinuria in febrile illnesses

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5
Q

Vaccinations at 8 weeks

A

6 in 1 (diphtheria, hep B, Hib, polio, tetanus, whooping cough
Rotavirus
MenB

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6
Q

Timing for late-onset GBS sepsis

A

Up to 3 months after birth

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7
Q

When would you give steroids in meningitis

A 
Never <3 months of age
Give dexamethasone if >3 months and: 
- frankly purulent CSF
- WCC>1000
- raised WCC + protein + bacteria on gram stain
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8
Q

Important differential if fever >5 days

A

Kawasaki disease

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9
Q

How to differentiate between a rigor and a febrile convulsion

A

Consciousness

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10
Q

Causative organism in Scarlet fever

A 
Streptococcus pyogenes (Group A beta-haemolytic strep)
Normally present in nasopharynx but may cause tonsillitis or pharyngitis (Scarlet fever evolves from this)
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11
Q

Spread of Scarlet fever

A

Respiratory droplet spread

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12
Q

Incubation period for Scarlet fever - when are they contagious?

A

1-7 days

During the active illness and the incubation period

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13
Q

Common age for Scarlet fever

A

Age 2-10 years (unlikely under 2 due to maternal antibody protection)

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14
Q

Common presentation of Scarlet fever

A

Sudden onset fever with tachycardia followed by typical rash 24-48 hours later
White strawberry tongue which then sheds (desquamation) to red strawberry tongue
Peeling skin of fingers and toes especially

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15
Q

Typical rash in Scarlet fever

A

Generalised erythema with pin-point, dark red spots overlying and a coarse/sandpaper texture
Typically affects neck, chest and scapular regions first before spreading to trunk and legs
Circumoral pallor

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16
Q

Treatment for Scarlet fever

A

Antibiotics - penicillin or azithromycin for 10 days
Rest and adequate fluids
Ibuprofen/paracetamol for symptom relief

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17
Q

What is Kawasaki disease

A

Systemic, autoimmune mediated vasculitis affecting small and medium sized vessels
Also known as mucocutaneous lymph node syndrome

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18
Q

Where is Kawasaki disease most common

A

Japan (and East Asia)

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19
Q

Diagnostic criteria for Kawasaki disease

A

Fever for >5 days and 4 of the following:
1. conjunctivitis
2. mucous membrane changes (e.g. strawberry tongue, dry and cracked lips)
3. cervical lymphadenopathy
4. widespread erythematous maculopapular rash
5. desquamation or oedema of feet/hands
Children will be very irritable

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20
Q

Phases of Kawasaki disease course of illness

A

Acute (1-2 weeks) - child is most unwell with fever, rash and lymphadenopathy
Subacute (2-8 weeks) - acute symptoms settle, skin peels and arthralgia sets in. Risk of CAAs
Convalescent (months+) - resolution of symptoms and biochemical results. Cardiac dysfunction may still occur

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21
Q

Most important possible complication of Kawasaki disease

A

Cardiac complications - coronary artery aneurysms

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22
Q

Treatment for Kawasaki disease

A

Aspirin + IV immunoglobulin

Follow up with echocardiograms

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23
Q

Where is group B strep commonly found

A

Vagina and rectum (20-40% of women in the UK)

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24
Q

Risk of baby developing GBS infection if found by vaginal swab at 35-37 weeks gestation

A

1 in 500

Higher risk if GBS detected in urine

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25
Q

3 complications of GBS infection in newborns

A

Sepsis
Pneumonia
Meningitis

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26
Q

Risk factors for early-onset neonatal GBS infection

A
  • intrapartum fever (>38C)
  • prematurity (<37/40)
  • prolonged ROM (>18hrs)
  • known GBS carrier
  • previous infant with GBS infection
  • GBS UTI during current pregnancy
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27
Q

Intrapartum management of GBS

A

Intrapartum abx prophylaxis (prevention of early-onset neonatal infection) - IV BenPen

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28
Q

Postpartum management of GBS

A

Measure CRP of babies starting abx
IV BenPen with gentamycin
?stopping abx at 36 hours if showing signs of response

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29
Q

Definition of Henoch-Schonlein purpura (HSP)

A

IgA-mediated autoimmune hypersensitivity vasculitis of childhood

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30
Q

Clinical features of HSP

A 
Skin purpura 
Arthritis
Abdo pain
GI bleeding 
Nephritis
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31
Q

Description of typical rash in HSP

A

Begins as red spots/bumps (hive-like appearance) rapidly changes to small, dark, purple bumps (palpable purpura) within first 24 hours
Lower legs, buttocks, elbows and knees
Symmetrical distribution

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32
Q

Treatment for HSP

A

Normally self-limiting condition therefore supportive treatment and prevention of complications
Monitor renal function - blood pressure, urinalysis, U&Es

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33
Q

Renal involvement in HSP

A

Up to 55% of children but is generally mild

Ranges from microscopic haematuria and mild proteinuria to nephrotic/nephritic syndrome and renal failure

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34
Q

Prognosis for HSP

A

Generally self-limiting and resolves within 4 weeks

Prognosis depends on severity of renal involvement

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35
Q

Definition of febrile convulsion

A

Seizures which occur in response to a rapid rise in temperature (fever >38C)

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36
Q

3 classifications of febrile convulsion

A
  1. simple febrile seizure
  2. complex febrile seizure
  3. febrile status epilepticus
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37
Q

Features of simple febrile seizure

A

Tonic clonic seizure lasting <15 mins
Don’t reoccur within 24hrs or within same febrile illness
No long-term neuro effects, no increased risk of epilepsy

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38
Q

Features of complex febrile seizure

A

Features of focal seizure
Lasts >15 mins
Reoccur within same febrile illness

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39
Q

What is febrile status epilepticus

A

Febrile seizure lasting >30 mins

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40
Q

Risk factors for reoccurrence of febrile seizure

A
  • young age at first seizure
  • first seizure occurs early in course of infection
  • low temp at first seizure (low threshold)
  • FHx
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41
Q

Differentials for seizures in children

A 
Epilepsy
Head injury 
Encephalitis
Hypoglycaemia
Hyperglycaemia
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42
Q

Common infections causing febrile seizures

A

Otitis media
Viral infections
Tonsillitis

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43
Q

Description of tonic-clonic seizure

A

Tonic phase = body is stiff and rigid for up to 60 seconds, incontinence and tongue biting may occur
Clonic phase = generalised convulsions and limb jerking

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44
Q

Management approach for simple febrile convulsions

A

Parental education and reassurance
Antipyretics in febrile illnesses, removal of excess clothing
Timing and describing seizure

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45
Q

Management of prolonged febrile seizure (>5 mins)

A

Rectal or buccal diazepam

Repeat at 5 mins

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46
Q

When to suspect (and treat) meningitis in a febrile seizure

A 
Systemically unwell, irritable or drowsy before seizure
GCS <15 one hour after
Neck stiffness
Non-blanching rash
Bulging fontanelle
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47
Q

Treatment of meningococcal disease

A

BenPen or cefotaxime

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48
Q

Criteria for moderate acute asthma in children

A
  • able to talk in sentences
  • oxygen over 92%
  • peak flow over 50% best/predicted
  • HR <140 (age 1-5) or <125 (5+)
  • RR <40 (age 1-5) or <30 (5+)
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49
Q

Criteria for severe acute asthma in children

A
  • can’t complete full sentences
  • oxygen under 92%
  • peak flow 33-50% best/predicted
  • HR >140 (age 1-5) or >125 (5+)
  • RR >40 (age 1-5) or >30 (5+)
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50
Q

Criteria for life-threatening acute asthma in children

A
  • exhaustion
  • hypotension
  • cyanosis
  • silent chest
  • poor resp effort
  • confusion
  • peak flow <33% best/predicted
  • oxygen under 92%
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51
Q

What is stridor

A

Inspiratory wheeze caused by an upper airway obstruction

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52
Q

Management of mild croup

A

Oral dexamethasone 0.15mg/kg single dose

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53
Q

Management of moderate croup

A

Oral dexamethasone 0.15mg/kg single dose and observe in ED for 2-3 hours
If worsening symptoms give nebulised adrenaline 5ml of 1:1000 and observe

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54
Q

Management of severe croup

A

Nebulised adrenaline 5ml of 1:1000 and oral/IV dexamethasone 0.15mg/kg
Oxygen by facemask

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55
Q

Definition of bronchiolitis

A

Inflammation and infection in the bronchioles (LRTI)

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56
Q

Cause of bronchiolitis

A

Respiratory syncytial virus (RSV) most commonly

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57
Q

What age group gets bronchiolitis

A

Under 6 months most common
Under 1 year old
Age 1-2 more rare, in children with underlying lung disease

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58
Q

Risk factors for severe disease in bronchiolitis

A 
Prematurity
Low birth weight
Mechanical ventilation as a neonate
Age <12 weeks (now)
Medical conditions: chronic lung disease, congenital heart disease, neuro disease, epilepsy, diabetes, immunocompromise, congenital airway defects, Downs
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59
Q

Pathophysiology of bronchiolitis

A

Virus invasion and inflammatory response causes swelling and mucus of the small airways. Young children have very small airways to begin with therefore this change causes significant impact on their breathing ability.

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60
Q

Course of illness in bronchiolitis

A

Begins as URTI - coryzal symptoms
Chest symptoms day 1-2
Peak of symptoms day 3-4
Symptoms generally resolve day 7-10

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61
Q

What are the signs of respiratory distress in infants

A 
Raised resp rate
Use of accessory muscles and head bobbing
Intercostal and subcostal recession
Tracheal tug
Grunting
Nasal flaring
Cyanosis
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62
Q

What is heard on auscultation of the chest in bronchiolitis

A

Wheeze and crackles

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63
Q

How may very young infants present differently in bronchiolitis

A

May present with apnoeas (periods of no breathing) and no other signs

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64
Q

Criteria for admission in bronchiolitis

A
  • aged <3 months
  • pre-existing conditions e.g. Downs, prematurity, CF
  • decreased feeding <75% normal
  • clinical dehydration
  • RR >70
  • oxygen <92%
  • respiratory distress
  • apnoeas
  • parents unable to cope/ living far from medical care
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65
Q

What is the general approach to managing bronchiolitis

A

Supportive - reassurance to parents, fluid intake, nasal suctioning if needed

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66
Q

When to give supplementary oxygen in bronchiolitis

A

Sats consistently below 92%

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67
Q

Criteria for discharge after bronchiolitis admission

A
  • clinically stable
  • taking adequate oral fluids
  • maintaining oxygen over 92% in air for >4 hours including a period of sleep
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68
Q

Immunoprophylaxis for bronchiolitis

A

Palivizumab (monoclonal antibody) - gives passive immunity to those at high risk of developing severe disease

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69
Q

Definition of viral-induced wheeze

A

Acute wheezy illness caused by viral infection

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70
Q

Cause of viral-induced wheeze

A

Respiratory syncytial virus (RSV)

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71
Q

Pathophysiology of viral-induced wheeze

A

Virus infection and inflammatory response leads to inflammation and oedema in airways. Also causes bronchoconstriction.

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72
Q

Difference between viral-induced wheeze and bronchiolitis

A

Viral-induced wheeze most common aged 1-3 whereas bronchiolitis is most common under 1
Viral-induced wheeze shows bronchoconstriction whereas bronchiolitis is ‘wet lungs’ i.e. mucus/oedema
This is related to the child’s developing immune system and different immune responses at different ages

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73
Q

How to distinguish between asthma and viral-induced wheeze

A

Asthma isn’t commonly diagnosed before age 5, VIW is most common under 3
Asthma shows atopic history, VIW doesn’t
VIW only occurs during viral infections whereas asthma is likely to have other triggers such as cold weather, dust, exercise`

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74
Q

Definition of asthma

A

Chronic inflammation of the bronchial mucosa and hyper-reactive airways resulting in bronchoconstriction and reversible airway narrowing

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75
Q

Differentials for asthma in chidlren

A

Transient early wheezers/ viral-induced wheeze (associated with viral infection, aged under 3)
Non-atopic wheezers (resolves by age ~5)

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76
Q

What is the management of viral-induced wheeze

A

Same as management of acute asthma in children

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77
Q

First-line treatments for acute asthma in children

A
  1. Oxygen (if <94%)
  2. Salbutamol
    - MDI + spacer: 10 puffs (100mcg)
    - nebs if needing O2: 2.5-5mg
  3. Ipratropium bromide
    - 250mcg nebs
  4. Steroids
    - oral prednisolone 10-40mg depending on age
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78
Q

Second-line treatments for acute asthma in children (not responding to first-line methods)

A
  1. IV salbutamol
    - IV bolus of 15mcg/kg over 10 mins
    - cont. IV infusion 1-2mcg/kg/min
  2. IV aminophylline
    - 5mg/kg bolus over 20 mins followed by cont. infusion at 1mg/kg/hr
  3. IV mag sulph (preferred)
    - up to 75mg/kg/day
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79
Q

Description of the wheeze heard in asthma

A

Expiratory polyphonic wheeze

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80
Q

4 tests used to investigate and diagnose suspected asthma in children

A
  1. fractional exhaled nitric oxide (FeNO)
  2. obstructive spirometry
  3. bronchodilator reversibility test
  4. peak flow variability
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81
Q

Level of FeNO which may indicate asthma diagnosis

A

35ppb (parts per billion) or more

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82
Q

What is fractional exhaled nitric oxide and why is it useful

A

FeNO
NO is produced by cells involved in the inflammation associated with atopic asthma therefore measuring this gives an idea of how much inflammation is occurring and how severe the atopic asthma is

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83
Q

Result of obstructive spirometry which may indicate asthma diagnosis

A

FEV1/FVC ratio <70%

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84
Q

Result of bronchodilator reversibility test which may indicate asthma diagnosis

A

Improvement in FEV1 of >12%

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85
Q

Result of peak flow variability testing which may indicate asthma diagnosis

A

Variability over 20%

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86
Q

Step-up algorithm to management of chronic asthma in children over 5

A
  1. SABA as required (salbutamol)
  2. regular preventer - low dose inhaled corticosteroids (ICS)
  3. add LABA (salmeterol) or LTRA (montelukast)
  4. increase ICS or add remaining LABA/LRTA
  5. refer to specialist, consider stopping LABA
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87
Q

Which trisomy is related to Downs syndrome

A

21 (extra chromosome)

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88
Q

Clinical features of Downs syndrome often spotted at birth

A
  • hypotonic
  • flat occiput
  • single palmar creases
  • incurved fifth finger
  • wide ‘sandal’ gap between big and second toes
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89
Q

Most common mechanism leading to trisomy 21

A 
Meiotic nondysjunction (94%)
Related to maternal age
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90
Q

Craniofacial appearance of Downs syndrome

A
  • round face and flat nasal bridge
  • upslanted palpebral fissures
  • epicanthic folds
  • brushfield spots in iris
  • small mouth and protruding tongue
  • small ears
  • flat occiput and third fontanelle
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91
Q

Medical problems associated with Downs syndrome which may be present at birth

A
  • congenital heart disease (40%)
  • duodenal atresia
  • Hirschsprung disease
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92
Q

Medical problems associated with Downs syndrome which may come later on in life

A
  • delayed motor milestones
  • learning difficulties
  • short stature
  • increased susceptibility to infections
  • hearing impairment from secondary otitis media
  • visual impairment
  • obstructive sleep apnoea
  • epilepsy
  • early onset Alzheimer’s
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93
Q

2 tests (after birth) to investigate for Downs syndrome

A

Rapid PCR

Rapid fluorescence in situ hybridization (FISH)

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94
Q

Which trisomy is associated with Edwards syndrome

A

Trisomy 18

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95
Q

Clinical features of Edwards syndrome

A
  • low birth weight
  • prominent occiput
  • small mouth and chin
  • short sternum
  • flexed, overlapping fingers
  • rocker-bottom feet
  • low-set and malformed ears
  • microcephaly
  • cleft lip and palate
  • malformation of sex organs
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96
Q

Complications associated with Edwards syndrome

A

Most die before or shortly after birth

  • congenital heart defects (>90%)
  • GI abnormalities e.g. hernia, pyloric stenosis
  • UG abnormalities e.g. horseshoe kidney, hydronephrosis
  • neuro e.g. hydrocephaly, severe learning disability
  • central apnoea (can cause death)
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97
Q

Trisomy associated with Patau syndrome

A

Trisomy 13

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98
Q

Clinical features of Patau syndrome

A
  • scalp defects
  • small eyes and other eye defects (cyclops)
  • cleft lip and palate
  • polydactyly
  • malformation of sex organs
  • ear malformations
  • rocker-bottom feet
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99
Q

Complications associated with Patau syndrome

A

Most die before or shortly after birth

  • congenital heart defects (80%)
  • severe learning disability
  • central apnoea
  • hearing impairment
  • GI abnormalities e.g. hernia
  • UG abnormalities e.g. polycystic kidneys
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100
Q

2 types of breath holding spells in children

A
  1. cyanotic/blue breath holding spells

2. reflex anoxic seizures

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101
Q

Description of a cyanotic/blue breath holding spell

A

An episode in which upset toddlers cry and (involuntarily) hold their breath on expiration leading to cyanosis. The child may lose consciousness but recovers quickly.

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102
Q

Description of a reflex anoxic seizure

A

After a trigger (e.g. pain, discomfort, minor head trauma, fright or fever), the vagus nerve sends strong signals to the heart to stop beating leading to pallor and loss of consciousness. Hypoxia may induce a tonic-clonic seizure but it is brief.

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103
Q

What is hyperekplexia

A

Whole body stiffening in response to a sudden noise or being touched/handled. Can be terminated by forced flexion of the neck.

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104
Q

Symptoms of reflux in babies

A
  • bringing up milk or being sick shortly after feeds
  • coughing/hiccupping during feeds
  • unsettled during feeding
  • swallowing or gulping after burping or feeding
  • not gaining weight (not keeping food down)
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105
Q

When can children with chicken pox return to school

A

After all vesicles have crusted over

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106
Q

When can children with rubella return to school

A

After four days from onset of rash

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107
Q

When can children with impetigo return to school

A

After lesions are crusted and healed or after 48 hours of antibiotics

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108
Q

When can children with measles return to school

A

After four days from onset of rash

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109
Q

When can children with Scarlet fever return to school

A

After 24 hours of antibiotics

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110
Q

Which paediatric rashes/skin infections don’t need to have time off school

A

Hand, foot and mouth
Molluscum contagiosum
Roseola infantum
Slapped cheek (fifth disease/parvovirus B19)

111
Q

Presentation of measles

A
  • prodrome of fever, malaise, anorexia, conjunctivitis, cough and coryzal symptoms
  • Koplik spots in mouth
  • rash: flat, red, non-itchy spots beginning on face and behind ears and may spread over whole body with palm/sole sparing
112
Q

What is immune thrombocytopaenia

A

Autoimmune condition leading to depleted platelet levels due to antibody production against platelets. May follow viral infection or (more rarely) vaccination.

113
Q

Common presentation of immune thrombocytopaenia

A

Petechiae or bruising of skin
Can show no symptoms, mild bleeding issues e.g. nosebleeds, haematuria or progress to GI bleeds or life-threatening intracranial haemorrhage

114
Q

Treatment for immune thrombocytopaenia

A

Most are mild and self-resolving just needing platelet monitoring and safety netting around trauma prevention and avoiding NSAIDs and aspirin
If more severe: pred, IV Ig, IV anti-D Ig, rituximab, dexamethasone
Emergency platelet transfusion if needed

115
Q

Benefits of breastfeeding for the baby

A

Reduces risk of:

  • infections
  • D&V
  • sudden infant death syndrome
  • obesity
  • CVD (adulthood)
  • necrotising enterocolitis
  • childhood leukaemia
116
Q

Benefits of breastfeeding for mother

A

Reduces risk of:

  • breast cancer
  • ovarian cancer
  • osteoporosis
  • CVD
  • obesity
  • T2DM
117
Q

Risk factors for developing neonatal jaundice

A
  • preterm
  • ethnicity: Asian, European, Native American
  • newborn factors: visible jaundice <24hrs of life, gestation <38/40, male, visible bruising
  • maternal factors: DM, >25y/o, exclusive breast feeding
  • previous sibling needing phototherapy
118
Q

epidemiology of physiological jaundice in newborns

A
  • occurs between day 2 and 10 of life
  • no underlying cause
  • breastfed > bottle fed
119
Q

How to distinguish physiological jaundice biochemically

A

Physiological jaundice is always unconjugated

120
Q

Pathophysiology of physiological jaundice in the newborn

A
  • neonates have a shorter RBC lifespan therefore bilirubin levels are higher
  • metabolism and excretion of bilirubin is slower
  • immature liver in preterm babies
121
Q

Criteria indicating abnormal (pathological) jaundice

A
  • occurs <24h birth
  • lasts >14 days in term babies
  • lasts >21 days in preterm babies
122
Q

Underlying disorders which cause jaundice due to increased bilirubin production

A
  • blood group incompatibility (ABO, Rhesus)
  • G6P deficiency
  • IVH
  • cephalohaematoma
  • polycythaemia
  • sepsis -> DIC
  • bruising
123
Q

Underlying disorders which cause jaundice due to decreased bilirubin clearance

A
  • extrahepatic biliary atresia
  • neonatal cholestasis: alpha-1-antitrypsin deficiency, cystic fibrosis
  • inborn errors: Gilbert syndrome, Crigler-Najjar syndrome
  • hypothyroidism, hypopituitarism
124
Q

Differentials for unconjugated jaundice in neonates

A
  • breastmilk jaundice
  • infection (UTI)
  • haemolysis (blood group incompatibility, G6PD)
  • hypothyroidism
  • high GI obstruction
  • Crigler-Najjar syndrome
125
Q

Differentials for conjugated jaundice in neonates

A
  • biliary atresia
  • choledochal cyst
  • congenital infection
  • inborn errors
  • alpha1-antitrypsin
  • galactosaemia
  • cystic fibrosis
126
Q

Diagnostic levels for unconjugated and conjugated hyperbilirubinaemia

A

Unconjugated hyperbilirubinaemia = >80% total bilirubin is unconjugated
Conjugated hyperbilirubinaemia = >20% of total bilirubin is conjugated

127
Q

How does phototherapy work for neonatal jaundice

A

Blue-green light converts unconjugated bilirubin in water soluble molecules that can be excreted

128
Q

Definition of prolonged jaundice

A

Jaundice lasting >14 days in term babies or >21 days in preterm babies

129
Q

Investigations for prolonged jaundice

A
  • general assessment: feeding, weight, stool and urine colour
  • (if well) split bilirubin test
  • if split test shows a hyperbilirubinaemia (unconjugated or conjugated) refer to paediatrician for further testing
130
Q

Further testing for conjugated hyperbilirubinaemia

A
  • repeat split bilirubin
  • LFTs
  • blood glucose
  • coagulation
131
Q

6 common congenital birthmarks

A
  • congenital melanocytic naevi (brown birthmark)
  • cafe au lait spots
  • mongolian spots
  • haemangioma
  • macular stains/salmon patches
  • port-wine stain
132
Q

Description of congenital melanocytic naevus`

A

Single- or multi- shaded, round- or oval- shaped, patches. May have increased hair growth (hypertrichosis)

133
Q

Description of cafe au lait spots and important note

A

Hyperpigmented skin patch with sharp border and diameter of >0.5cm
Up to 3 are normal in Caucasians, up to 5 are normal in Afro-Caribbean’s - any more may indicate neurofibromatosis

134
Q

Description of Mongolian blue spots

A

Bluish-grey patches commonly found on back or buttocks

135
Q

Description of Macular stains/Salmon patches

A

Small, flat patches of pink or red skin with poorly defined borders

136
Q

Description of haemangioma (strawberry naevus)

A

Raised, pink or purple patch with clearly defined border. Waxy look and surface may contain telangiectasia.

137
Q

Description of port-wine stain

A

Large, flat patch or purple or dark red skin with well-defined borders. Begins as flat surface but may become more bumpy.

138
Q

in which age group is appendicitis most common

139
Q

how does appendicitis present in children

A

acute abdo pain
classic pain distribution not as common and may be vague
watery diarrhoea and vomiting in infants

140
Q

management of appendicitis in children

A

appendicectomy if high clinical suspicion

antibiotic treatment: cefuroxime and metronidazole

141
Q

complications of appendicitis

A

perforation and peritonitis
appendix mass
abscesses
wound infection

142
Q

what is mesenteric adenitis

A

inflammation of the lymph nodes in the abdomen

143
Q

common age for mesenteric adenitis presentation

A

under 16yo

144
Q

what causes mesenteric adenitis

A

viral infection commonly

more rarely bacterial infection

145
Q

common presentation of mesenteric adenitis

A

mild abdo pain
following period of coryzal symptoms/viral illness e.g. sore throat, runny nose
may have fever, malaise, nausea, diarrhoea

146
Q

management of mesenteric adenitis

A

analgesia and rest (viral illness)

if bacterial, antibiotics accordingly

147
Q

what is intussusception

A

telescoping or invagination of a section of bowel into a distal segment, leading to obstruction

148
Q

risk factors for intussusception

A
  • male gender
  • conditions pre-disposing e.g. Meckel’s diverticulum, polyps, haemangiomas, tumours, appendix inflammation, CF, coeliac, Crohn’s
  • viral infection
  • rotavirus vaccine
149
Q

common age of presentation of intussusception

A

under 1yo

peak age 5-10 months

150
Q

example of a non-pathological lead point in intussusception

A

viral infection e.g. rotavirus, adenovirus

151
Q

example of a pathological lead point in intussusception

A

pre-existing condition:

  • Meckel’s diverticulum
  • HSP
  • lymphoma
  • CF
152
Q

common presentation of intussusception

A

sudden onset colicky abdominal pain (waves every 10-20 mins)

  • bile stained vomiting
  • redcurrant jelly stools
  • palpable ‘sausage-shaped’ mass often in RUQ
153
Q

key ultrasound finding in intussusception

A

doughnut/target sign

154
Q

management of intussusception

A
  • resuscitation (‘drip and suck’): IV fluids and NG tube
  • radiological intervention: air or barium enema
  • laparotomy to reduce or resect bowel if peritonitic/perforated
155
Q

complications of intussusception

A

ischaemia and necrosis of the bowel
sepsis, septicaemia
haemorrhage
perforation and peritonitis

156
Q

management of paediatric constipation

A
  • acute disimpaction using osmotic laxatives
  • reassurance and advice to parents and child
  • diet and lifestyle modifications: fluid, fibre, exercise
  • behavioural modifications
  • consider child abuse (neglect)
157
Q

what is testicular torsion

A

torsion or twisting of the spermatic cord causing occlusion of testicular blood vessels

158
Q

what structural abnormality is associated with testicular torsion

A

‘Bell-clapper’ deformity = lack of normal fixation of posterolateral aspect of tunica vaginalis meaning testes are free to swing and rotate within TV

159
Q

which testicle is more commonly affected by torsion

160
Q

common presentation of testicular torsion

A
  • sudden, severe pain and swelling in one testis with redness of skin
  • lower abdo pain, N&V
  • onset often during sport or physical activity
161
Q

clinical sign indicating testicular torsion

A

absence of cremasteric reflex (stroking of inside thigh causes retraction of testis on same side - not present)

162
Q

2 types of testicular torsion and associated group who gets it

A

intravaginal - Bell-clapper deformity

extravaginal - neonates

163
Q

first-line investigation for testicular torsion

A

US integrated with colour doppler

164
Q

management of testicular torsion

A

possible manual reduction (outwards rotation) should see immediate relief - if not, emergency surgical intervention and bilateral orchiopexy
orchidectomy may be required if testicle is no longer viable

165
Q

complications of testicular torsion

A

infarction and necrosis of affected testicle - possible orchidectomy required (prosthesis fitted)
subfertility or infertility - unlikely if still have remaining testicle

166
Q

definition of meningitis

A

inflammation of the meninges

167
Q

aetiology of meningitis

A

caused by viral infection more commonly (generally less severe) but can be caused by bacteria (more severe - bacterial until proven otherwise)

168
Q

common causative bacteria in neonatal meningitis

A
  • group B strep
  • listeria monocytogenes
  • e. coli
169
Q

common causative bacteria of meningitis in infants and young children

A
  • haemophilus influenzae type B (HIB)
  • neisseria meningitidis (<4, not vaccinated)
  • strep pneumoniae
170
Q

common causative bacteria of meningitis in adults and older children

A
  • strep pneumoniae
  • HIB
  • neisseria meningitidis
  • gram-neg bacilli e.g. klebsiella, pseudomonas
171
Q

common symptoms of meningitis

A
  • stiff neck (uncommon in <1yo or low GCS)
  • non-blanching rash
  • back rigidity
  • photophobia
  • leg pain
172
Q

common signs of meningitis

A
  • non-blanching rash
  • bulging fontanelle (infants)
  • CR >2s, cold peripheries
  • unusual skin colour
  • altered mental state
173
Q

what is Kernig’s sign

A

meningitis - pain and resistance on passive knee extension with hips fully flexed

174
Q

what is Brudzinski’s sign

A

meningitis - hips flex on bending the head forward

175
Q

management of meningitis

A
  • supportive treatment with analgesia, antipyretics, nutritional support and hydration
  • metabolic/circulatory disturbances corrected
  • antibiotics (blind therapy then confirmed)
  • if older than 3 months, give dexamethasone stat
176
Q

dose of dexamethasone for meningitis

A

(>3m)

0.15mg/kg (max 10mg) QDS for 4 days

177
Q

what is the initial blind abx therapy for meningitis

A

under 3 months old: cefotaxime + ampicillin/amoxicillin IV

over 3 months old: ceftriaxone IV

178
Q

abx management of n. meningitidis meningitis

A

7+ days IV ceftriaxone

179
Q

abx management of s. pneumoniae meningitis

A

14 days IV ceftriaxone

180
Q

abx management of hib meningitis

A

10 days IV ceftriaxone

181
Q

abx management of group b strep meningitis

A

14+ days IV cefotaxime

182
Q

abx management of listeriosis meningitis

A

7 days IV amoxicillin/ampicillin + gentamycin then further 14 days IV amoxicillin/ampicillin

183
Q

bloods to order in suspected meningitis

A

FBC, CRP, coagulation screen, blood culture, PCR for n. meningitidis, blood glucose, ABG, U&E

184
Q

other investigations (not bloods) to order in suspected meningitis

A
  • lumbar puncture
  • CXR
  • urine culture
  • nasopharyngeal swabs
  • stool virology
  • CT is adverse clinical features
185
Q

when is lumbar puncture contraindicated in suspected meningitis

A
  • signs of increased intracranial pressure e.g. reduced consciousness, extreme headache, frequent fits
  • focal neurology
  • severe shock/sepsis
186
Q

definition of pneumonia

A

infection of the lung tissue which causes inflammation and filling of sputum in the alveoli

187
Q

risk factors for pneumonia in children

A
  • <5yo
  • premature (24-28 weeks gestation)
  • seasonal variation: peaks in december and august
188
Q

common causative organisms for pneumonia in newborns

A
  • GBS
  • gram-neg enterococci and bacilli
  • myobacterium tuberculosis
189
Q

common causative organisms for pneumonia in infants and young children

A
  • RSV
  • parainfluenza
  • influenza
  • strep. pneumoniae
  • h. influenza
  • staph. aureus
  • mycobacterium tuberculossi
190
Q

4 common causative organisms for pneumonia in children older than 5

A
  • mycoplasma pneumonia
  • strep. pneumonia
  • chlamydia pneumonia
  • mycobacterium tuberculosis
191
Q

common symptoms of pneumonia

A
  • high fever (>39)
  • cough (wet and productive)
  • increased WOB
  • lethargy
  • poor feeding
  • delirium
  • generally unwell
192
Q

common signs of pneumonia

A
  • tachypnoea
  • tachycardia
  • hypoxia (<95%)
  • cyanosis
  • focal coarse crackles
  • decreased breath sounds
  • bronchial breathing
  • dullness of percussion
  • signs of resp distress
193
Q

investigations to order for suspected pneumonia

A
  • obs
  • nasopharyngeal aspirate for viral PCR and bacterial cultures
  • FBC, CRP
  • blood cultures
194
Q

management of pneumonia at home

A
  • antipyretics
  • fluids to prevent dehydration
  • safety netting
  • course of antibiotics
195
Q

management of pneumonia in hospital

A
  • oxygen therapy by nasal cannula or face mask (aim >92%)
  • fluids (oral -> NG -> IV)
  • antibiotics
196
Q

abx choice in pneumonia

A

first line = amoxicillin 7-14 day
penicillin allergic or atypical = …thromycin
oral unless not tolerated or signs of septicaemia

197
Q

what is pyloric stenosis

A

hypertrophy of the pyloric muscle causing obstruction of the gastric outlet

198
Q

risk factors for pyloric stenosis

A
  • male
  • maternal FHx
  • affected siblings
199
Q

common symptoms of pyloric stenosis

A

2-8 weeks of age

  • projectile vomiting in otherwise well child after feeding
  • continuous hunger after vomiting
  • weight loss/poor weight gain, failure to thrive
  • dehydration late stage
200
Q

common signs of pyloric stenosis

A
  • peristalsis observed in abdomen
  • firm, olive shaped mass felt in RUQ
  • signs of dehydration
201
Q

ABG finding in pyloric stenosis

A

metabolic alkalosis with hypochloraemic and hypokalaemic state

202
Q

investigations to do in suspected pyloric stenosis

A
  • abdo exam shows olive shaped mass in RUQ
  • test feed to show wave of peristalsis and projectile vomiting
  • ABG
  • USS shows thickened pyloric muscle (>4mm)
  • barium meal shows string sign of elongated and narrowed pyloric sphincter
203
Q

management of pyloric stenosis

A
  • correct fluid and electrolyte imbalances
  • insert NG tube to decompress stomach
  • laparoscopic pyloromyotomy
204
Q

how is weight faltering defined

A

sustained drop of two centiles or below the 0.4th centile or BMI <2nd centile

205
Q

5 categories for causes of weight faltering

A
  1. inadequate intake
  2. inadequate retention
  3. malabsorption
  4. failure to utilize nutrients
  5. increased requirements
206
Q

examples of inadequate intake causing weight faltering

A
  • availability of food
  • psychosocial deprivation e.g. maternal depression or interaction
  • neglect or child abuse
  • impaired suck/swallow e.g. cerebral palsy, cleft palate
  • chronic illness e.g. crohns, CF
207
Q

examples of inadequate retention causing weight faltering

A

vomiting

severe GORD

208
Q

examples of malabsorption leading to weight faltering

A 
coeliac
CF
cows milk intolerance
short gut syndrome
previous NEC
209
Q

examples of failure to utilize nutrients leading to weight faltering

A 
Downs
IUGR
extreme prematurity
congenital infection
congenital hypothyroidism
210
Q

examples of increased requirements leading to weight faltering

A 
thyrotoxicosis
CF
malignancy
HIV/immune deficiency
congenital heart disease
211
Q

definition of precocious puberty

A

development of secondary sexual characteristic before 8yo in females and 9yo in males

212
Q

subtypes of precocious puberty

A
  • premature breast development (thelarche)
  • premature pubic hair development (pubarche or adrenarche)
  • isolated premature menarche
213
Q

risk factors for precocious puberty

A
  • female
  • exposure to CNS radiotherapy
  • obesity
  • afrocaribbean ethnicity
  • exposure to exogenous sex hormones
214
Q

what tool is used to help assess development of secondary sexual characteristics

A

Tanner staging

215
Q

2 main mechanisms of precocious puberty

A 
GnRH dependent, true precocious puberty (high LH > high FSH)
GnRH independent (low FSH and LH)
216
Q

pathophysiology of GnRH dependent precocious puberty

A

premature activation of hypothalamic-pituitary-gonadal axis caused by:

  • idiopathic (sporadic or familial) in 80% of girls and 40% of boys
  • CNS abnormalities e.g. tumours, trauma, hydrocephalus
  • hypothyroidism
217
Q

pathophysiology of GnRH independent precocious puberty

A

increased sex hormone production not related to maturation of HPG axis - gonad matures without GnRH stimulation

  • congenital adrenal hyperplasia
  • tumours: HCG-secreting tumours in liver, ovarian tumour
  • severe hypothyroidism
  • exogenous oestrogen or androgen exposure
218
Q

investigations in suspected precocious puberty

A

?GnRH dependent or independent

  • head circ, weight and height
  • sex steroid levels
  • LH and FSH levels
  • TFTs
  • HCG
  • US (ovaries, testes, adrenal glands)
  • hand and wrist XR for bone age
  • brain MRI
  • GnRH stimulation test
219
Q

what is the treatment for congenital adrenal hyperplasia

A

glucocorticoids

220
Q

what is leukaemia

A

cancer of the blood-forming tissue, usually bone marrow, leading to overproduction of abnormal white cells

221
Q

4 categories of leukaemia

A
  1. acute lymphoblastic leukaemia
  2. acute myeloid leukaemia
  3. chronic myeloid leukaemia
  4. chronic lymphoblastic leukaemia
222
Q

which is the most common leukaemia in children

A

acute lymphoblastic leukaemia (78%)

223
Q

when does acute myeloid leukaemia most commonly present

A

infants (<2yo)

224
Q

which leukaemia is very rare in children

A

chronic lymphoblastic leukaemia

225
Q

describe the differentiation of blood cells

A

stem cell differentiates into a) lymphoid stem cell or b) myeloid stem cell

a) lymphoid stem cell becomes lymphoblast which differentiates in either B or T lymphocyte
b) myeloid stem cell becomes either platelet, RBC or myeloid blast (which becomes monocyte or neutrophil)

226
Q

when does acute lymphoblastic leukaemia most commonly present

227
Q

when does chronic myeloid leukaemia commonly present

A

2 peaks: children <1yo and early teenage years

228
Q

symptoms of leukaemia

A
  • malaise, fatigue, lethargy
  • prolonged/recurrent fever
  • irritability
  • failure to thrive
  • SOB, reduced exercise tolerance
  • dizziness, palpitations
  • bleeding issues e.g. epistaxis, bruising
  • bone/joint pain (leg)
  • constipation
  • prolonged cough
  • headache
  • nausea & vomiting
  • repeated or severe childhood infections
229
Q

signs of leukaemia due to bone marrow infiltration

A
  • anaemia (pallor, lethargy)
  • neutropaenia (infection)
  • thrombocytopaenia (bruising, petechiae, epistaxis)
  • bone pain
230
Q

signs of leukaemia due to reticulo-endothelial infiltration

A
  • hepatosplenomegaly

- lymphadenopathy

231
Q

signs of leukaemia due to other organ infiltration

A
  • CNS (headaches, vomiting, nerve palsies)

- testes (testicular enlargement)

232
Q

investigations for leukaemia in primary care

A
  • FBC (pancytopaenia if bone marrow is infiltrated)

- blood film

233
Q

investigations for leukaemia in secondary care

A
  • bone marrow aspiration and biopsy
  • imaging (extent of disease)
  • immunophenotyping and cytogenic analysis
  • lumbar puncture (if suspected CNS infiltration)
234
Q

management of acute lymphoblastic leukaemia

A
  • high-intensity chemo via central venous catheter

- myeloablation + allogenic bone marrow transplant

235
Q

management of acute myeloblastic leukaemia

A
  • intensive chemotherapy
236
Q

management of chronic myeloid leukaemia

A
  • myeloablative haematopoietic stem cell transplantation
237
Q

what is cerebral palsy

A

group of disorders causing permanent but non-progressive abnormalities of motor function and posture

238
Q

aetiology of cerebral palsy

A
  • damage to the immature brain: vascular, hypoxic-ischaemic, teratogenic, genetic, infective, toxin, metabolic or trauma
  • most common in antenatal period (24 weeks gestation to term)
  • associated with neonatal encephalopathy (HIE or sepsis)
  • post-neonatal common causes are meningitis, infection and head injury
239
Q

what area of the brain is affected in hemiplegic spastic cerebral palsy

A

unilateral motor cortex (arm and leg affected on one side)

240
Q

what area of the brain is affected in diplegic cerebral palsy

A

bilateral medial motor cortex (both legs > both arms affected)

241
Q

what area of the brain is affected in quadriplegic cerebral palsy

A

bilateral entire motor cortex (all 4 limbs)

242
Q

what area of the brain is affected in athetoid cerebral palsy

A

basal ganglia

243
Q

what area of the brain is affected in ataxic cerebral palsy

A

cerebellum

244
Q

description of movement in spastic type cerebral palsy

A
  • intermittently increased tone

- pathological reflexes

245
Q

description of movement in athetoid cerebral palsy

A
  • increased activity (hyperkinesia)

- ‘stormy movement’

246
Q

description of movement in ataxic type cerebral palsy

A
  • loss of orderly muscle coordination

- movements performed with abnormal force, rhythm or accuracy

247
Q

which type of cerebral palsy is most common

A

bilateral (diplegia or quadriplegia) spastic type cerebral palsy

248
Q

antenatal risk factors for cerebral palsy

A

pre-term birth, congenital malformations, multiple births, intrauterine infection, chorioamnionitis, toxic/teratogenic agents, maternal infection/illness

249
Q

perinatal risk factors for cerebral palsy

A

low birth weight, neonatal encephalopathy, neonatal sepsis

250
Q

postnatal risk factors for cerebral palsy

A

meningitis, intracranial haemorrhage, trauma, infection, hyperbilirubinaemia, hypoxia, seizures

251
Q

developmental milestone delays which may indicate cerebral palsy

A
  • not sitting by 8 months
  • not walking by 18 months
  • early asymmetry of hand function (preference) before 1 year old
252
Q

signs of cerebral palsy which may present at 12-18 months

A
  • abnormal posture/movement
  • usual fidgety or asymmetrical movements
  • abnormal tone (floppiness or stiffness)
  • abnormal motor development: head control, rolling, crawling
  • feeding difficulties
253
Q

common conditions associated with cerebral palsy

A
  • learning disability
  • communication difficulties
  • emotional and behavioural issues
  • visual or hearing impairment
  • chronic constipation
  • epilepsy
254
Q

investigations to rule out other differentials when suspecting cerebral palsy

A
  • TFTs
  • chromosomal analysis
  • pyruvate and lactate levels (mitochondrial cytopathies)
  • organic and amino acid levels (inborn errors)
  • CSF protein, lactate and pyruvate (neonatal asphyxia)
255
Q

4 examples of medical treatment of spasticity

A
  1. diazepam
  2. baclofen
  3. botulinum toxin A
  4. phenol and ethyl alcohol
256
Q

key principles for preventing cerebral palsy

A
  • recognition and treatment of maternal iodine
  • prevention of kernicterus associated with rhesus isoimmunisation
  • prolong pregnancy in preterm labour (e.g. tocolytics)
  • improve neonatal ICU
257
Q

what is ASD

A

autistic spectrum disorder

developmental condition causing an impairment of social interaction, communication and flexible behaviour

258
Q

what is Aspergers

A

normal intelligence and ability to function in everyday life but displays difficulties in reading emotions and responding to others

259
Q

differentials to consider when suspecting autism

A
  • deafness
  • general learning disability
  • childhood disintegrative disorder (Heller’s disease)
  • Rett syndrome: X-linked neurodevelopmental condition involving loss of spoken language and hand use
260
Q

genetic risk factors for autism

A
  • chromosomal anomalies
  • affected sibling
  • metabolic errors such as PKU
261
Q

environmental risk factors for autism

A
  • advanced prenatal age
  • exposure to teratogens
  • maternal diabetes
  • antenatal infection: rubella, influenza
  • low birth weight
  • birth asphyxia
  • abnormally short gestational length
262
Q

clinical features of autism relating to social interaction

A
  • lack of eye contact
  • smiling delay
  • avoiding physical contact
  • inability to read non-verbal cues
  • difficulty establishing friendships
  • no desire to share attention e.g. playing with others
  • lack of awareness of social norms
263
Q

clinical features of autism relating to communication

A
  • delayed, absence or regression of language development
  • lack of appropriate non-verbal communication
  • difficulty with imaginative or imitative behaviour
  • repetitive use of words or phrases
264
Q

clinical features of autism relating to behaviour

A
  • greater interest in objects, number or patterns than people
  • repetitive movements
  • highly specific and narrow interests/hobbies
  • strong preference for fixed routine
  • unusual reactions to sensory stimuli
  • extremely restricted food preferences
265
Q

4 assessment tools for autism

A
  1. autism diagnostic interview, revise (ADI-R)
  2. diagnostic interview for social and communication disorders (DISCO)
  3. development, dimensional and diagnostic interview
  4. AQ-10 (adults)
266
Q

diagnostic criteria for autism

A

6+ symptoms across all 3 areas (communication, social interaction and behaviour)
observed in different environments e.g. home, school, clinic

267
Q

management options for autism

A
  • behavioural and psychological interventions
  • speech and language therapy
  • interventions to support social skills
268
Q

what is ADHD

A

attention deficit hyperactivity disorder
extreme end of hyperactivity and inability to concentrate
affects ability to carry out every day tasks, develop normal skills and perform well at school
must be consistent across various settings

269
Q

risk factors for ADHD

A
  • low birth weight
  • preterm birth
  • acquired brain injury
  • epilepsy
  • lead poisoning
  • iron deficiency
  • maternal health problems
  • substance misuse
  • presence of other mental health or neurodevelopmental disorders
270
Q

2 categories of clinical features of ADHD

A
  • inattention

- hyperactivity and impulsivity

271
Q

criteria for clinical features of ADHD to meet for diagnosis

A
  • some symptoms present before 12 years of age
  • some symptoms present in two or more settings
  • evidence that symptoms interfere with social, school or work functioning
  • symptoms not better explained by another mental disorder
272
Q

rating scale used for adhd

273
Q

examples of medication used in ADHD

A
  • methylphenidate (ritalin)
  • dexamfetamine
  • atomoxetine

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